Body water is divided into cellular and extracellular compartments. It is possible to induce drinking behavior by selectively reducing the fluid volume of either compartment. The renin-angiotensin system has been implicated as a mediator of the water intake seen following many of the manipulations which induce physiological conditions associated with a reduced extracellular volume. In order to be able to accept angiotensin as a hormone of thirst, several significant questions must be answered. First, it is necessary to know how angiotensin interacts with the central nervous system. Are the neural receptors which are sensitive to circulating levels of angiotensin located in the periphery or does the hormone act directly on sensitive areas within the brain? Second, to what extent is extracellular thirst mediated by the renal renin-angiotensin system? Third, does a recently discovered renin- angiotensin system which is endogenous to the brain have a functional role in thirst? The application of a molecular analog of angiotensin which acts as a competitive inhibitor will aid in solving these problems. The site of angiotensin action to induce thirst can be assessed by determining if intracranially applied antagonist is more or less effective than systemically delivered antagonist in blocking the effects of systemically infused exogenous angiotensin. The roles of the renal angiotensin system and of the brain renin-angiotensin system in thirst can be evaluated by observing the effect on water intake of systemically and centrally applied inhibitor following various thirst challenges such as water deprivation, caval ligation, hypovolemia induced by subcutaneous hyperoncotic colloid, B-adrenergic activation, and cellular dehydration.